Iron is an essential element for all cells and plays important role in neurodevelopment. Putamen is the site of the highest iron concentration in the brain. Whether an elevated iron intake, might contribute to structural and cellular damage in the putamen or not remains currently unclear.
To detect effects of high iron intake during the gestational and lactation periods on the putamen of offspring rats.
16 pregnant rats were randomly equally divided into two groups; the control group received distilled water orally daily from the eighth day of pregnancy till the 20th day postnatally, and the treated group received ferrous gluconate dissolved in distilled water at a dose of 15 mg/kg body weight orally daily for the same period. Offspring rats included in this study were at the ages of newborn, 10 days, and 20 days. The brains from 6 male offspring from each age group were dissected, fixed, and processed for light microscopy, transmission electron microscopy, tyrosine hydroxylase immunohistochemistry, and morphometry.
The putamen in the three ages of the iron-treated group had vacuolations in the neuropil, and the neurons showed shrunken nuclei, vacuolations, damaged mitochondria with marked loss of cell organelles as compared to the control. Neurodegenerative changes were increased with increasing the age of rats. In addition, there was a reduction of positive TH immunoreactivity and a decrease in the cell count in the iron-treated group as compared to the control.
Iron excess during pregnancy and lactation produced neuronal degeneration in the putamen of the growing rats.
Background: Stent manufacturers always record stent shortening data while they do not record stent elongation data. The aim of this study is to identify both stent shortening and elongation occurring after deployment in the coronary arteries and know their percentage.
Results: The length of coronary stents was measured by intravascular ultrasound (IVUS) by (1) edge-to-edge (E-E) length, measured from the appearance of the first distal strut to the last proximal strut, and (2) area-to-area (A-A) length, measured from the first distal struts seen at more than one IVUS quadrant to the last proximal struts seen at more than one IVUS quadrant. Stent shortening was defined as both E-E and A-A lengths were shorter than the manufacturer box-stated length (shortened group). Stent elongation was defined as both E-E and A-A lengths were longer than the manufacturer box-stated length (elongated group), otherwise unchanged group. Consecutive 102 stents deployed in ischemic patients were included. Stent elongation was detected in 67.6% (69 stents), and shortening was detected in 15.7% (16 stents), while unchanged stents were detected in 16.7% (17 stents). Although the 3 groups had similar box-stated length and predicted foreshortened length, they had significantly different measurements by IVUS, p<0.001 for each comparison. Differences from box-stated length were 1.9±1.4mm, -1.4±0.4mm, and 0.4±0.3mm, respectively, p<0.001. The elongated group had significantly longer differences from the corresponding box-stated and predicted foreshortened lengths, while the shortened group had significantly shorter differences from the corresponding box-stated length and similar foreshortened length. By multinomial regression analysis, the plaque-media area and stent deployment pressure were the independent predictors of the stent length groups, p=0.015 and p=0.026, respectively.
Conclusions: Change in stent length is not only shortening-as mentioned in the manufacturer documents-but also stent elongation. Stent elongation is dominant, and the most important predictors of longitudinal stent changes are plaque-media area and stent deployment pressure.
Keywords: IVUS; Stent elongation and shortening; Stent length.
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